Causes of Respiratory Failure I
• Lung tissue
– Pneumonia
– Pulmonary
hemorrhage
– Pulmonary edema
– Respiratory distress
syndrome (hyaline
membrane disease)
HMD
wet lung
meconial aspiration
congenital pneumonia
Adults and children: Acute respiratory distress syndrome (ARDS)
Oxygenation
Lung volumes
Pulm. compliance
Mortality: 25 - 35%
Newborn: Infant respiratory distress syndrome (iRDS)
Mechanical
ventilation
Ventilator
induced lung
injury
CLD: 15 - 25%
MRI signal intensity from non-dependent to dependent regions
The water burden of the lung makes the lung of the preterm infant,
despite surfactant treatment,vulnerable to VILI
4-day-old, 26-week gestation infant
2-day-old, 38-week gestation infant
Adams EW
AJRCCM 2002; 166:397–402
Nonhomogeneous Lung Disease
The pathophysiology shared by these diseases is
nonuniform lung involvement where certain lung units
are nearly normal while other areas are markedly
abnormal.
A strategy that is effective in opening damaged
areas may result in overinflation and trauma to
more normal areas of the lung.
Diffuse “Homogeneous” Lung Disease
The goals of assisted ventilation in this
group of patients are to improve lung inflation,
compliance and ventilation/perfusion matching while
avoiding barotrauma or compromise of cardiac output.
The best approach = The extended sigh
(stepwise increase and decrease of PEEP using the lowest VT possible)
Required Monitoring:
SaO2, PaO2
PaCO2 and/or endtidal CO2
Hemodynamics
PEEP titration
The oxygenation
response: Can it
be used?
Recruitment
"static" compliance:
Cst =
tidal volume
static PIP (Pplat) - PEEP
Burns D J Trauma 2001;51:1177-81
Overdistension
PEEP titration: O2 and CO2 response
in a lung injury model of surfactant depletion
Steps of 5
cmH2O to
35/20
20/5
PEEP 20
PEEP 15
PEEP 10
PEEP 5
Pressure control ventilation
20/5
ETT disconnection
O2-improvement = Shunt improvement =
a) recruitment
VA
b) flow diversion
VA
PaO2
PaCO2
PaO2
PaCO2
O2-improvement does not exclude overinflation
Prevalent overinflation = dead space effect
1
2
1
1
1
–
PEEP 5
PaO2 and PaCO2 increase
PEEP 15
Gattinoni L (2003)
Volume (l)
Allowable Vt and disease severity
ALI
(surfactant
depleted
lung)
severe
(A)RDS
Airway pressure (cmH2O)
Transition from CMV to HFOV
1) Pplat approaching 25 cmH2O after PEEP trial (recruitment)
and / or PEEP > 12 cmH2O
2) Reduction of Vt < 5 required to match Pplat limits
3) “uncomfortably” high pCO2 or low pH
(level dependent from additional pathologies)
Rationale for HFOV-based lung protective strategies
CMV
HFOV
CMV
HFOV
1. HFOV uses very small VTs.
This allows the use of higher EELVs to achieve greater
levels of lung recruitment while avoiding injury from
excessive EILV.
2. Respiratory rates with HFOV are much higher than with
CV.
This allows the maintenance of normal or near-normal
PaCO2 levels, even with very small Vts.
The concept of volume recruitment during HFO
Suzuki H Acta Pediatr Japan 1992; 34:494-500
Continuous blood gas monitoring during HFO
12 11 10 9
11
CDP: 13
Overdistention
Collapse
Causes of Respiratory Failure II
Lung hypoplasia syndromes
–
–
–
–
Congenital diaphragmatic hernia
Potter syndrome
prolonged rupture of membranes
Hydrops fetalis
The common variable in this group of infants is small,
often abnormal lungs. This is associated to:
- Difficult CO2 elimination
- Pulmonary hypertension (PPHN)
Congenital diaphragmatic hernia
Gentle ventilation (peak pressure limitation)
“Permissive” hypercapnia  resp acidosis
May worsen PPHN
iNO
HFO
ECMO
“Versus” VILI (baro- volutraumatisme)
Congenital diaphragmatic hernia
Accept
ductal
shunting as
long as RV
function is
not
impaired!
Bohn D
Am J Respir Crit Care Med 2002; 166: 911–915
Survival rates in CDH
Bohn D
Am J Respir Crit Care Med 2002; 166: 911–915
The Scandinavian Experience with CDH
“Geneva” attitude
Surfactant (-)
NO +/- (Cardiac US!)
HFOV +++ (early)
ECMO (-)
Sakri H
Pediatr Surg Int (2004) 20: 309–313
Causes of Respiratory Failure III
Conducting airways
• Aspiration (before or
after birth)
• Congenital
malformation
• Tracheal fistula
Extra- and intrathoracic airway obstruction
+
Stridor
+
From Pérez Fontán JJ, 1990
Classical pathological conditions that may
lead to a difficult to ventilate situation
Severe airway compression / malacia
No PEEP
PEEP 10cmH2O
courtesy from Quen Mok, Great Ormond Street Hospital for Children, London
Severe airway compression
Once you can ventilate these patients (with high
PEEP) they are usually difficult to extubate
My advice:
Keep a high PEEP on spontaneous ventilation, reduce pressure
support and extubate from a high PEEP (ev. to CPAP or NIV)
External PEEP in obstructive lung disease (PEEP-trial)
VT = 6 mL/kg
RR = 6/min
VT = 6 mL/kg
RR = 9/min
VT = 9 mL/kg
RR = 6/min
Caramez MP
VT = 9 mL/kg
RR = 9/min
Crit Care Med 2005; 33:1519 –1528
External PEEP in obstructive lung disease (PEEP-trial)
“paradoxical”
response
Biphasic
response
Caramez MP
Classical
overinflation
response
Crit Care Med 2005; 33:1519 –1528
HFOV in severe
airway
obstruction
Duval E
Pediatric Pulmonology
2000: 30:350–353
Causes of Respiratory Failure IV
Air leak syndromes
• Pneumothorax
• Bronchopulmonary
fistula
• PIE
CMV
HFOV
Tracheal pressure (cmH2O)
Endinspiration
CMV
Endexpiration
HFOV
PIP
PEEP
Classical indication for HFV
- because of small pressure swings
PIE, bronchopleural fistula, pneumothroax
Recruit to improve oxygenation and in order to lower the
FiO2 needed – then reduce the airway pressures to the
lowest level needed (air leak will often cease)
References:
Shen Chest 2002;121;284-6
Mayes Chest. 1991; 100:263-4
Rubio Intensive Care Med. 1986;12:161-3
One sided intubation or airway blocking by inserted balloon catheters is
almost never required even in severe airleak
(this was just a nice idea to get a case report)
Causes of Respiratory Failure V
Pulmonary perfusion
• Congenital heart
disease
• Persistent fetal
circulation
31 6/7 wks GA, 1000 g GA (small for GA)
1 course of prenatal steroids 12 hours before delivery
Presents with respiratory distress at birth:
RR 64, indrawing, SO2 84% at RA
CPAP trial with fast increasing O2 requirements (> 60%)
Venous and arterial umbilical catheter
First art BGA: pH 7.09, PCO2 11 kPa (83 mmHg), pO2 4.36
Intubation
Vent settings: TCPL, RR 60, PEEP 5, PIP 18
Poor sats persists: SO2 78% under FiO2 80%
PIP 24, PEEP 8, RR 60
Art BGA:
no real change in SO2
(SaO2 82 % , FiO2 100%)
pH 7.11, pCO2 10 kPa, pO2 3.33, BE –3.6
A: Surfactant?
B: HFOV?
C: Other?
Switch to HFOV: CDP 19, Pressure Ampl 46, Freq 12 Hz
SO2 80 %, FiO2 100%
Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8
A: Surfactant?
B: Increase CDP?
C: Other?
CDP 19, Pressure Ampl 46, Freq 12 Hz
SO2 80 %, FiO2 100%
Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8
CDP 19, Pressure Ampl 46, Freq 12
SO2 80 %, FiO2 100%
Art BGA: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8
CDP 14, Pressure Ampl 34, Freq 15
SO2 92 %, FiO2 can be lowered fast to 40%
Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6
Diagnosis and what next?
CDP 14, Pressure Ampl 34, Freq 15
SO2 92 %, FiO2 40%
Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6
CDP 14, Pressure Ampl 34, Freq 15 Hz
SO2 92 %, FiO2 can be lowered fast to 40%
Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6
SO2 78 %
CDP 13, Pressure Ampl 30, Freq 15 Hz
SO2 91 %, FiO2 can be furter lowered to 25%
Art BGA: pH 7.42, pCO2 4.4, pO2 3.50, BE –2
SO2 74 %
iNO 8 ppm
CDP 13, Pressure Ampl 25, Freq 15 Hz
SO2 94 %, FiO2 can be furter lowered to 21%
Art BGA: pH 7.39, pCO2 4.87, pO2 3.59, BE –2.3
Echo cardiac
6 hours later (after refixation of ETT) rapid drop in saturation
to values around 60 to 65% under FiO2 of 100%,
hemodynamic stable (BP 49 / 30)
A) Increase in airway pressures for recruitment?
BGA:
B)
Surfactant
C) Increase iNO concentration
D) Other
CDP 13, Pressure Ampl 25, Freq 15 Hz
CDP 13, Pressure Ampl 25, Freq 15 Hz, FiO2 100%, iNO 12 ppm
Stepwise increase in CDP up to 20
Lactate:
SO2 72% pre and postductal
Art BGA: pH 7.22, pO2 3.56, pCO2 8.0, BE - 3
2.2
Gradually increase in P-Ampl to 46
Surfactant
SO2 varies around 65 to 75% on FiO2 100%, iNO 12 ppm
Art BGA: pH 7.1, pCO2 5.0, pO2 2.36, BE - 5
4.5
CDP 20, Pressure Ampl 48, Freq 10 Hz, FiO2 100%, iNO 12 ppm
SO2 varies around 55 to 75%
Art BGA: pH 6.97, pCO2 10.0, pO2 2.86, BE – 12, Lactate 8.6
A) Increase iNO, B) switch to CMV
C) change HFO settings, D) second dose of surfactant
CDP reduction from 20 to 14
Sat immediately improves to 90%,
allowing to reduce FiO2 to 60 then 40 %
Anticipate!
A) I have to reduce iNO
B) I lower further CDP
C) I change other settings – which one?
D) Excellent work, I need a coffee now!
Reduce pressure amplitude immediately when lowering CDP
(coming of overdistension will render oscillation swings more effective!)
Pressure amplitude from 48 to 30 (visible wiggeling)
Art BGA: pH 7.39, pCO2 3.4, pO2 6.26, BE – 10
CDP reduction from 14 to 10, P-amplitude to 24, FiO2 to 21%
PPHN with:
Closed ductus
1) R-L shunt across the FO
 severe hypoxemia
2) RV dilatation and failure
 poor CO
NO yes
Open ductus
1) Moderate mainly
postductal hypoxemia
+ ev R-L shunt FO
2) In general good CO
NO may lead to L-R shunt
with pulmonary flooding
R-L shunt and RV dilatation before iNO
Shunt inversement under iNO
RDS and PPHN in the newborn infant:
Nitric oxide effect
Right to left shunt without iNO
PA
Duct
Ao
Left to right shunt on iNO
PA
Duct
Ao
Indication: not poor postductal oxgygenation
but signs of poor cardiac output
Take home messages
It is not always iRDS that causes hypoxemia in the
preterm infant
If you don’t know what to do next with your ventilator settings
reduce your airway pressures first
Try to anticipate changes in respiratory mechanics and gas
exchange before turning knobs on your ventilator
Pressure – Flow – Time - Volume
Time constant: T = Crs x Rrs
To short Ti and/or Te will lead to inefficient alveolar
ventilation and risk of intrinsic PEEP
Adapt your respirator rate (Ti and/or Te) to the stage
and mechanical characteristics of lung disease
The saying “ we ventilate at 60/min” is a testimony of no understanding
Take home messages
In pulmonary disease lung volumes (functional for
gas exchange) are usually reduced – the “need” for
smaller VT than physiological VT is a logical
consequence of this
When you try to recruit a lung you need to have
appropriate monitoring (CO2!)
If you don’t know what to do next with your ventilator settings
reduce your airway pressures first
Try to anticipate changes in respiratory mechanics and gas
exchange before turning knobs on your ventilator
In situations of difficult ventilation an
analytical approach is required
1) What are the characteristics of airway or lung disease?
- type (etiology) of disease
- stage of disease, history
- mechanical behaviour
2) Is the problem “physician”-induced?
3) Which bedside method (monitoring) might be helpful
during a PEEP trial?